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Article ; Online: Evaluation of possible role of fluoride in pathogenesis of oral submucous fibrosis: A pilot study.

Arakeri, Gururaj / Rao Us, Vishal / Patil, Shekar / Kunigal, Sateesh / Reddy, Roopa / Krishnan, Murugesan / Hale, Beverley / Brennan, Peter A

Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology

2024 Volume 53, Issue 3, Page(s) 226–231

Abstract: Background: Oral submucous fibrosis (OSMF) is a potentially malignant disorder. Although areca nut chewing is an established risk factor, its low prevalence among nut chewers indicates additional factors likely facilitates pathogenesis. We recently ... ...

Abstract	Background: Oral submucous fibrosis (OSMF) is a potentially malignant disorder. Although areca nut chewing is an established risk factor, its low prevalence among nut chewers indicates additional factors likely facilitates pathogenesis. We recently demonstrated high fluoride levels in smokeless tobacco products and hypothesized a potential pathological role of fluoride in OSMF. Further exploring this novel role, this study compared fluoride levels in tissue, serum, and saliva samples from OSMF patients and healthy controls. Methods: The ethically approved study included 25 clinically confirmed OSMF patients and 25 healthy matched controls. OSMF cases underwent buccal mucosal incisional biopsy, while controls had buccal mucosa tissue sampling during third molar removal. Fasting venous blood and unstimulated saliva were collected. Fluoride levels were analysed using ion chromatography and expressed as median (IQR). Results: OSMF cases showed significantly higher fluoride concentrations compared with controls in tissue biopsies (30.1 vs. 0 mg/kg, p < 0.0001), serum (0.4 vs. 0 mg/L, p = 0.005) and saliva (1.3 vs. 0 mg/L, p < 0.0001). Majority (68%) of controls had undetectable fluoride levels across all samples. Tissue fluoride weakly correlated with OSMF severity (r = -0.158, p = 0.334). Conclusion: The preliminary findings demonstrated increased tissue fluoride levels in OSMF patients compared with healthy controls. Along with a previous study showing high fluoride content in smokeless tobacco products, these findings provided early evidence suggesting fluoride could play a contributory role in OSMF pathogenesis. Further large-scale investigation is warranted to definitively establish whether the association between fluoride exposure and OSMF is indicative of causation.
MeSH term(s)	Humans ; Oral Submucous Fibrosis/pathology ; Fluorides/adverse effects ; Pilot Projects ; Mouth Mucosa/pathology ; Tobacco, Smokeless/adverse effects
Chemical Substances	Fluorides (Q80VPU408O)
Language	English
Publishing date	2024-02-28
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	1021270-x
ISSN	1600-0714 ; 0904-2512
ISSN (online)	1600-0714
ISSN	0904-2512
DOI	10.1111/jop.13527
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Withdrawal: Blockade of tumor growth due to matrix metalloproteinase-9 inhibition is mediated by sequential activation of β1-integrin, ERK, and NF-κB.

Bhoopathi, Praveen / Chetty, Chandramu / Kunigal, Sateesh / Vanamala, Sravan K / Rao, Jasti S / Lakka, Sajani S

The Journal of biological chemistry

2020 Volume 295, Issue 45, Page(s) 15426

Language	English
Publishing date	2020-10-28
Publishing country	United States
Document type	Journal Article ; Retraction of Publication
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.W120.016338
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Article ; Online: (i) TNM staging for head and neck cancers.

Vishal Rao, U S / Shetty, Sameep S / Kudpaje, Akshay / Rao, Gururaj A / Kunigal, Sateesh S

Oral oncology

2019 Volume 97, Page(s) 133–134

MeSH term(s)	Head and Neck Neoplasms/pathology ; Humans ; Neoplasm Staging/methods
Language	English
Publishing date	2019-08-27
Publishing country	England
Document type	Letter
ZDB-ID	1120465-5
ISSN	1879-0593 ; 0964-1955 ; 1368-8375
ISSN (online)	1879-0593
ISSN	0964-1955 ; 1368-8375
DOI	10.1016/j.oraloncology.2019.08.016
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Zs.A 4869: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.A 456: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)

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Book ; Online ; Thesis: Urokinase-activated Stat1 mediates antiproliferative effect in vascular smooth muscle cells cocultered with monocytes

Kunigal, Sateesh Sreenivasan

2003

Abstract: Atherosclerosis, urokinase-type plasminogen activator and receptor (uPA-uPAR) system, signal transducer and activator of transcription 1 (Stat1), ... ...

Author's details	von Sateesh Sreenivasan Kunigal
Abstract	Atherosclerosis, urokinase-type plasminogen activator and receptor (uPA-uPAR) system, signal transducer and activator of transcription 1 (Stat1), coculture
Language	English
Size	Online-Ressource (87 p. = 5387 Kb)
Edition	[Elektronische Ressource]
Publisher	Technische Informationsbibliothek u. Universitätsbibliothek
Publishing place	Hannover
Document type	Book ; Online ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Hannover, 2003
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Book ; Online ; Thesis: Urokinase-activated Stat1 mediates antiproliferative effect in vascular smooth muscle cells cocultered with monocytes

Kunigal, Sateesh Sreenivasan

2003

Abstract: Atherosclerosis, urokinase-type plasminogen activator and receptor (uPA-uPAR) system, signal transducer and activator of transcription 1 (Stat1), ... ...

Author's details	von Sateesh Sreenivasan Kunigal
Abstract	Atherosclerosis, urokinase-type plasminogen activator and receptor (uPA-uPAR) system, signal transducer and activator of transcription 1 (Stat1), coculture
Language	English
Size	Online-Ressource (87 p. = 5387 Kb)
Edition	[Elektronische Ressource]
Publisher	Technische Informationsbibliothek u. Universitätsbibliothek
Publishing place	Hannover
Document type	Book ; Online ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Hannover, 2003
Database	Former special subject collection: coastal and deep sea fishing

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Article ; Online: Mammalian lysine histone demethylase KDM2A regulates E2F1-mediated gene transcription in breast cancer cells.

Rizwani, Wasia / Schaal, Courtney / Kunigal, Sateesh / Coppola, Domenico / Chellappan, Srikumar

PloS one

2014 Volume 9, Issue 7, Page(s) e100888

Abstract: It is established that histone modifications like acetylation, methylation, phosphorylation and ubiquitination affect chromatin structure and modulate gene expression. Lysine methylation/demethylation on Histone H3 and H4 is known to affect transcription ...

Abstract	It is established that histone modifications like acetylation, methylation, phosphorylation and ubiquitination affect chromatin structure and modulate gene expression. Lysine methylation/demethylation on Histone H3 and H4 is known to affect transcription and is mediated by histone methyl transferases and histone demethylases. KDM2A/JHDM1A/FBXL11 is a JmjC-containing histone demethylase that targets mono- and dimethylated Lys36 residues of Histone H3; its function in breast cancer is not fully understood. Here we show that KDM2A is strongly expressed in myoepithelial cells (MEPC) in breast cancer tissues by immunohistochemistry. Ductal cells from ductal carcinoma in situ (DCIS) and infiltrating ductal carcinoma (IDC) show positive staining for KDM2A, the expression decreases with disease progression to metastasis. Since breast MEPCs have tumor-suppressive and anti-angiogenic properties, we hypothesized that KDM2A could be contributing to some of these functions. Silencing KDM2A with small interfering RNAs demonstrated increased invasion and migration of breast cancer cells by suppressing a subset of matrix metalloproteinases (MMP-2, -9, -14 and -15), as seen by real-time PCR. HUVEC cells showed increased angiogenic tubule formation ability in the absence of KDM2A, with a concomitant increase in the expression of VEGF receptors, FLT-1 and KDR. KDM2A physically bound to both Rb and E2F1 in a cell cycle dependent manner and repressed E2F1 transcriptional activity. Chromatin immunoprecipitation (ChIP) assays revealed that KDM2A associates with E2F1-regulated proliferative promoters CDC25A and TS in early G-phase and dissociates in S-phase. Further, KDM2A could also be detected on MMP9, 14 and 15 promoters, as well as promoters of FLT1 and KDR. KDM2A could suppress E2F1-mediated induction of these promoters in transient transfection experiments. These results suggest a regulatory role for KDM2A in breast cancer cell invasion and migration, through the regulation of E2F1 function.
MeSH term(s)	Breast Neoplasms/pathology ; Cell Cycle ; Cell Line, Tumor ; Cell Movement ; Disease Progression ; E2F1 Transcription Factor/genetics ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; F-Box Proteins/genetics ; F-Box Proteins/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Jumonji Domain-Containing Histone Demethylases/genetics ; Jumonji Domain-Containing Histone Demethylases/metabolism ; Matrix Metalloproteinases/metabolism ; Neoplasm Invasiveness ; Neovascularization, Pathologic/metabolism ; Receptors, Vascular Endothelial Growth Factor/metabolism ; Retinoblastoma Protein/metabolism ; Transcription, Genetic ; Up-Regulation ; Vascular Endothelial Growth Factor Receptor-1/metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism
Chemical Substances	E2F1 Transcription Factor ; E2F1 protein, human ; F-Box Proteins ; Retinoblastoma Protein ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; KDM2A protein, human (EC 1.14.11.27) ; FLT1 protein, human (EC 2.7.10.1) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1) ; Vascular Endothelial Growth Factor Receptor-1 (EC 2.7.10.1) ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1) ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2014-07-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0100888
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book ; Thesis: Urokinase-activated Stat1 mediates antiproliferative effect in vascular smooth muscle cells cocultered with monocytes

Kunigal, Sateesh Sreenivasan

2003

Author's details	von Sateesh Sreenivasan Kunigal
Language	English
Size	VII, 76 Bl, Ill., graph. Darst
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Hannover, 2003
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Nicotine, IFN-γ and retinoic acid mediated induction of MUC4 in pancreatic cancer requires E2F1 and STAT-1 transcription factors and utilize different signaling cascades

Kunigal Sateesh / Ponnusamy Moorthy P / Momi Navneet / Batra Surinder K / Chellappan Srikumar P

Molecular Cancer, Vol 11, Iss 1, p

2012 Volume 24

Abstract: Abstract Background The membrane-bound mucins are thought to play an important biological role in cell–cell and cell–matrix interactions, in cell signaling and in modulating biological properties of cancer cell. MUC4, a transmembrane mucin is ... ...

Abstract	Abstract Background The membrane-bound mucins are thought to play an important biological role in cell–cell and cell–matrix interactions, in cell signaling and in modulating biological properties of cancer cell. MUC4, a transmembrane mucin is overexpressed in pancreatic tumors, while remaining undetectable in the normal pancreas, thus indicating a potential role in pancreatic cancer pathogenesis. The molecular mechanisms involved in the regulation of MUC4 gene are not yet fully understood. Smoking is strongly correlated with pancreatic cancer and in the present study; we elucidate the molecular mechanisms by which nicotine as well as agents like retinoic acid (RA) and interferon-γ (IFN-γ) induce the expression of MUC4 in pancreatic cancer cell lines CD18, CAPAN2, AsPC1 and BxPC3. Results Chromatin immunoprecipitation assays and real-time PCR showed that transcription factors E2F1 and STAT1 can positively regulate MUC4 expression at the transcriptional level. IFN-γ and RA could collaborate with nicotine in elevating the expression of MUC4, utilizing E2F1 and STAT1 transcription factors. Depletion of STAT1 or E2F1 abrogated the induction of MUC4; nicotine-mediated induction of MUC4 appeared to require α7-nicotinic acetylcholine receptor subunit. Further, Src and ERK family kinases also mediated the induction of MUC4, since inhibiting these signaling molecules prevented the induction of MUC4. MUC4 was also found to be necessary for the nicotine-mediated invasion of pancreatic cancer cells, suggesting that induction of MUC4 by nicotine and other agents might contribute to the genesis and progression of pancreatic cancer. Conclusions Our studies show that agents that can promote the growth and invasion of pancreatic cancer cells induce the MUC4 gene through multiple pathways and this induction requires the transcriptional activity of E2F1 and STAT1. Further, the Src as well as ERK signaling pathways appear to be involved in the induction of this gene. It appears that targeting these signaling pathways might inhibit the expression of MUC4 and prevent the proliferation and invasion of pancreatic cancer cells.
Keywords	Mucin 4 ; Pancreatic cancer ; Cell proliferation and invasion invasion ; Src Kinase ; Akt pathway. ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2012-04-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Book ; Online ; Thesis: Urokinase-activated Stat1 mediates antiproliferative effect in vascular smooth muscle cells cocultered with monocytes

Kunigal, Sateesh Sreenivasan [Verfasser]

2003

Author's details	von Sateesh Sreenivasan Kunigal
Keywords	Medizin, Gesundheit ; Medicine, Health
Subject code	sg610
Language	English
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Nicotine, IFN-γ and retinoic acid mediated induction of MUC4 in pancreatic cancer requires E2F1 and STAT-1 transcription factors and utilize different signaling cascades.

Kunigal, Sateesh / Ponnusamy, Moorthy P / Momi, Navneet / Batra, Surinder K / Chellappan, Srikumar P

Molecular cancer

2012 Volume 11, Page(s) 24

Abstract: Background: The membrane-bound mucins are thought to play an important biological role in cell-cell and cell-matrix interactions, in cell signaling and in modulating biological properties of cancer cell. MUC4, a transmembrane mucin is overexpressed in ... ...

Abstract	Background: The membrane-bound mucins are thought to play an important biological role in cell-cell and cell-matrix interactions, in cell signaling and in modulating biological properties of cancer cell. MUC4, a transmembrane mucin is overexpressed in pancreatic tumors, while remaining undetectable in the normal pancreas, thus indicating a potential role in pancreatic cancer pathogenesis. The molecular mechanisms involved in the regulation of MUC4 gene are not yet fully understood. Smoking is strongly correlated with pancreatic cancer and in the present study; we elucidate the molecular mechanisms by which nicotine as well as agents like retinoic acid (RA) and interferon-γ (IFN-γ) induce the expression of MUC4 in pancreatic cancer cell lines CD18, CAPAN2, AsPC1 and BxPC3. Results: Chromatin immunoprecipitation assays and real-time PCR showed that transcription factors E2F1 and STAT1 can positively regulate MUC4 expression at the transcriptional level. IFN-γ and RA could collaborate with nicotine in elevating the expression of MUC4, utilizing E2F1 and STAT1 transcription factors. Depletion of STAT1 or E2F1 abrogated the induction of MUC4; nicotine-mediated induction of MUC4 appeared to require α7-nicotinic acetylcholine receptor subunit. Further, Src and ERK family kinases also mediated the induction of MUC4, since inhibiting these signaling molecules prevented the induction of MUC4. MUC4 was also found to be necessary for the nicotine-mediated invasion of pancreatic cancer cells, suggesting that induction of MUC4 by nicotine and other agents might contribute to the genesis and progression of pancreatic cancer. Conclusions: Our studies show that agents that can promote the growth and invasion of pancreatic cancer cells induce the MUC4 gene through multiple pathways and this induction requires the transcriptional activity of E2F1 and STAT1. Further, the Src as well as ERK signaling pathways appear to be involved in the induction of this gene. It appears that targeting these signaling pathways might inhibit the expression of MUC4 and prevent the proliferation and invasion of pancreatic cancer cells.
MeSH term(s)	Cell Line, Tumor ; Cell Proliferation/drug effects ; Drug Synergism ; E2F1 Transcription Factor/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Interferon-gamma/pharmacology ; Janus Kinases/metabolism ; Mucin-4/genetics ; Nicotine/pharmacology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Promoter Regions, Genetic/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Nicotinic/metabolism ; STAT1 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Transcriptional Activation/drug effects ; Tretinoin/pharmacology ; src-Family Kinases/metabolism
Chemical Substances	E2F1 Transcription Factor ; Mucin-4 ; Receptors, Nicotinic ; STAT1 Transcription Factor ; Tretinoin (5688UTC01R) ; Nicotine (6M3C89ZY6R) ; Interferon-gamma (82115-62-6) ; Janus Kinases (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
Language	English
Publishing date	2012-04-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1476-4598
ISSN (online)	1476-4598
DOI	10.1186/1476-4598-11-24
Database	MEDical Literature Analysis and Retrieval System OnLINE

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